In a normal human eye, light coalesces to a central point on the retina, which is responsible for capturing all of the light rays and processing them to be sent to the optic nerve. Infrared light with a wavelength >700 nm is known to cause damage to the retina and the frontal eye, creating a physiological threat to anyone that comes into contact with IR emitting lasers. Studies show that near infrared red (NIR) light can induce resistance to apoptosis in human retinal cells. In normal cells, under ambient light, protection against apoptosis is mediated by nitric oxide (NO) induced elevations in cGMP, which activate cGMP-dependent protein kinase I (PKGI) isozymes. PKGI phosphorylates BAD, preventing it from binding BCL-XL, leading to decreased apoptosis. To verify that an increase of NO-stimulated apoptosis is caused by exposure to red light, intracellular NO was measured using DAF-FM in exposed and unexposed cells immediate, 1, 2, and 3 hr post-exposure to red light (632 nm, 2.88 J/cm2). Preliminary data shows that immediately after exposure to NIR light, there is a marginally significant increase in NO levels in comparison to unexposed cells (p=0.03). These data will be verified. Future directions include determining if external sources of NO can also inhibit apoptosis.
